Evidence map›Paper›PMID 25347734›Full record

ArticleOncogene2015

The human oncoprotein and chromatin architectural factor DEK counteracts DNA replication stress.

A Deutzmann, M Ganz, F Schönenberger, J Vervoorts, F Kappes, E Ferrando-May

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.6field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 46 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

A DeutzmannBioimaging Center, Department of Biology, University of Konstanz, Konstanz, Germany.
M GanzBioimaging Center, Department of Biology, University of Konstanz, Konstanz, Germany.
F SchönenbergerBioimaging Center, Department of Biology, University of Konstanz, Konstanz, Germany.
J VervoortsInstitute of Biochemistry and Molecular Biology, Medical School, RWTH Aachen University, Aachen, Germany.
F KappesInstitute of Biochemistry and Molecular Biology, Medical School, RWTH Aachen University, Aachen, Germany.
E Ferrando-MayBioimaging Center, Department of Biology, University of Konstanz, Konstanz, Germany.ORCID 0000000255678690
University of Konstanz · DERWTH Aachen University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA replication stress is a major source of DNA strand breaks and genomic instability, and a hallmark of precancerous lesions. In these hyperproliferative tissues, activation of the DNA damage response results in apoptosis or senescence preventing or delaying their development to full malignancy. In cells, in which this antitumor barrier is disabled by mutations (for example, in p53), viability and further uncontrolled proliferation depend on factors that help to cope with replication-associated DNA damage. Replication problems preferentially arise in chromatin regions harboring complex DNA structures. DEK is a unique chromatin architectural factor which binds to non-B-form DNA structures, such as cruciform DNA or four-way junctions. It regulates DNA topology and chromatin organization, and is essential for the maintenance of heterochromatin integrity. Since its isolation as part of an oncogenic fusion in a subtype of AML, DEK has been consistently associated with tumor progression and chemoresistance. How DEK promotes cancer, however, is poorly understood. Here we show that DEK facilitates cellular proliferation under conditions of DNA replication stress by promoting replication fork progression. DEK also protects from the transmission of DNA damage to the daughter cell generation. We propose that DEK counteracts replication stress and ensures proliferative advantage by resolving problematic DNA and/or chromatin structures at the replication fork.

Indexed as

DNA ReplicationAphidicolinBlotting, WesternCell Line, TumorCell ProliferationCell SurvivalChromatinChromosomal Proteins, Non-HistoneDNA DamageDose-Response Relationship, DrugEnzyme InhibitorsHeLa CellsHumansHydroxyureaMicroscopy, FluorescenceOncogene ProteinsAphidicolinChromatinChromosomal Proteins, Non-HistoneDEK protein, humanEnzyme InhibitorsHydroxyureaOncogene ProteinsPoly-ADP-Ribose Binding Proteins

Identifiers

PMID25347734
OpenAlexW2013193271

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.